HISTORY, CURRENT ILLNESS AND PHYSICAL EXAMINATION
A 26-year-old woman with no relevant past history except for well-controlled extrinsic asthma, who came to the emergency department for a febrile syndrome of 2 weeks' duration accompanied by general malaise, generalised arthromyalgia, headache and epigastralgia. He reported having started with this clinical condition after returning from a trip to Southeast Asia. One week before the consultation, he started with diarrhoea without pathological products. In addition, about 72 hours before admission, he presented continuous chest pain with pleuropericardial characteristics, which persisted at the time of assessment. He reported having been correctly vaccinated for the trip and had followed the health recommendations.
On arrival he presented with a low-grade fever (temperature 37.5oC). Skin pallor and general state of health, with rhythmic tachycardia at 140 beats per minute and blood pressure of 90/60 mmHg. Adequate basal saturation. No heart murmurs, pulmonary crackles or oedema in the lower limbs.

COMPLEMENTARY TESTS
Among the complementary tests performed in the initial assessment, we highlight the following:
Electrocardiogram: sinus tachycardia at 122 bpm with complete right bundle branch block (unknown) and ST elevation in the antero-septal aspect.
Portable chest X-ray: normal CTI. Discrete vascular redistribution, absence of pleural effusion or infiltrates.
Urgent laboratory tests (with normal values from the reference laboratory): pH 7.42 (7.35-7.45), creatinine 0.55 mg/dl (0.5-0.9), potassium 4.20 mmol/l (3.5-5.0), troponin I 30.52 μg/l (0.0 - 0.06), CK 871 IU/l. C-reactive protein 119.90 mg/l (0.1-10.0), NT-proBNP 13114 pg/ml (10-125). Lactate 2.2 mmol/l. Leukocytes 14.26 x10E3/μl (4.0-11.5) with neutrophils 10.27 x10E3/μl. Haemolobin 12.8 g/dl. INR 1.02.
Urgent transthoracic echocardiogram: moderately hypertrophic left ventricle with oedematous appearance and moderately depressed systolic function (subjective LVEF 35-40%). Right ventricle normal in size and function. Mildly moderate mitral regurgitation.
Minimal tricuspid insufficiency. No pericardial effusion, normal inferior vena cava.
During admission, the following tests were performed:
Serology: no relevant findings.
Blood cultures: negative.
Urine cultures: negative.
Pharyngeal smear and tracheal exudate: negative. ASLO: negative.
Endomyocardial biopsy: endomyocardial biopsy (3 fragments) with interstitial lymphohistiocytic infiltrates with myofibrillar damage, compatible with myocarditis.
ECG at discharge: sinus rhythm at 70 bpm. Wide QRS (150 ms) with morphology of complete right bundle branch block (RBBB). Generalised low voltage.
Echocardiography at discharge: left ventricle of normal dimensions, with moderate systolic dysfunction and global hypokinesia, although more pronounced at septal level. Global longitudinal Strain 12.8%. Normal right ventricle. Minimal mitral insufficiency. No tricuspid insufficiency. No pericardial effusion. Normal IVC.
Cardiac MRI: findings compatible with myocarditis. Slightly reduced global contractility (LVEF 47%). Thinning, hypokinesia and increased signal in STIR sequences and basal anteroseptal midventricular enhancement. Late enhancement of the lateral wall of the right ventricle. Mild pericardial effusion.
Renal and hepatic function and biomarkers of myocardial damage at discharge: creatinine 1.3 mg/dl.
Total bilirubin 1.4 mg/dl. GGT 51 U/l. Maximum troponin I 102 μg/l. NT-proBNP maximum of 110000 pg/ml, at discharge 4259 pg/ml.

CLINICAL EVOLUTION
After being assessed by the cardiology team, it was decided to transfer her to the acute cardiac care unit for close monitoring, where she presented poor initial evolution with criteria of cardiogenic shock, both clinical and analytical, so inotropic and vasoactive support treatment was started. An endomyocardial biopsy was performed, confirming the diagnosis of lymphocytic myocarditis, and it was decided to administer intravenous corticosteroids (three doses of methylprednisolone).
In the first hours of admission, the patient began with slow ventricular tachycardia with haemodynamic instability and incessant behaviour, despite treatment with intravenous antiarrhythmics and several attempts at electrical cardioversion. It was decided by consensus with the shock team to implant an intra-aortic balloon pump (IABP), with subsequent peripheral veno-arterial ECMO (extracorporeal membrane oxygenation) cannulation. The patient also required renal replacement therapy in the first days of admission due to acute renal failure.

After 5 days of mechanical circulatory support and in view of the favourable evolution, ECMO and IABP were gradually withdrawn. The patient was transferred to the cardiology ward to continue her evolution and start the titration of neurohormonal medication for heart failure with reduced ejection fraction. Control echocardiography at discharge showed improvement in ventricular function with moderate dysfunction and magnetic resonance imaging showed findings compatible with myocarditis.
The patient was discharged after three weeks of admission with a diagnosis of cardiogenic shock secondary to fulminant lymphocytic myocarditis (histopathological diagnosis), but none of the serologies, multiple cultures or other samples were able to identify a specific aetiological agent.
At the office evaluation more than one year later, the patient had recovered ventricular function and was in NYHA functional class I. She was maintained on neurohormonal treatment. Neurohormonal treatment for systolic dysfunction has been maintained.

DIAGNOSIS
Refractory cardiogenic shock (INTERMACS 1, SCAI E) with need for mechanical circulatory support (ECMO + IABP).
Fulminant lymphocytic myocarditis. Heart failure with depressed ejection fraction, recovered after one year of evolution with neurohormonal treatment. CF I NYHA.
Acute renal failure (Cardiorenal syndrome type I), resolved.
